June 13, 2017 by Casey Carr
By: Binoy Mistry MD
Created by a lack of balance between lactate production and metabolism
Type A Lactic Acidosis – Tissue hypo-perfusion resulting from hypovolemia, cardiac failure, sepsis, cardiac or respiratory arrest, carbon monoxide poisoning, etc.
Type B Lactic Acidosis – NO evidence of systemic hypo-perfusion. Includes toxin-induced impairment of cellular metabolism, regional areas of ischemia, impaired pyruvate dehydrogenase activity, impaired conversion of lactate, etc.
- Diabetes Mellitus – 3 mechanisms: Metformin, DKA – likely related to hypovolemia, D-lactic acid as a metabolite of acetone and dihydroxyacetone phosphate (DKA)
- Malignancy – pathogenesis not well understood. Possibly due to increased production by neoplastic cells
- Alcoholism – Decreased lactate hepatic clearance, oxidation of ethanol generates NADH (shifts pyruvate to lactate production)
- Mitochondrial dysfunction – congenital or acquired defects, drug-related. (ex. Propofol, linezolid, ART meds), Cyanide toxicity
- Beta-agonists – Exact mechanism unclear – possible increased pyruvate production, increase in glycogenolysis and glycolysis. 2 small prospective studies and multiple case reports have described lactate elevation after inhaled or IV Beta-agonist use. Unclear exact amount of lactate elevation.
- Thiamine deficiency – impaired pyruvate dehydrogenase activity
- Seizures, severe exercise – increased O2 demand
Take Home Message:
- Be aware that other things apart from hypo-perfusion can cause lactic acidosis
- Interpret lab values and imaging in the context of the patient in front of you
- Saying your lactate of 5.0 is due to albuterol should be a diagnosis of exclusion!
- Dodda VR, PS. Can Albuterol Be Blamed for Lactic Acidosis? Respiratory Care. 2012;57(12):2115-2118
- Kraut JA, Madias NE. Lactic Acidosis. N Engl J Med. 2014;371(24):2309-2319